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126
▲
Figure 6–17. Cellulitis. (Used, with permission, from
Lindy Fox, MD.)
group A beta-hemolytic streptococci and S aureus. Rarely,
gram-negative rods or even fungi can produce a similar
picture. In otherwise healthy persons, the most common
portal of entry for lower leg cellulitis is interdigital tinea
pedis with fissuring. Other predisposing conditions are
prior episodes of cellulitis, chronic edema, venous insufficiency with secondary edema, lymphatic obstruction,
saphenectomy, and other perturbations of the skin barrier.
Bacterial cellulitis is almost never bilateral.
CMDT 2025
CHAPTER 6
» Clinical Findings
A. Symptoms and Signs
Cellulitis begins as a tender small patch. Swelling, erythema, and pain are often present. The lesion expands over
hours, so that time from onset to presentation is usually
6–36 hours. As the lesion grows, the patient becomes more
ill with progressive chills, fever, and malaise. Lymphangitis
and lymphadenopathy are often present. If septicemia
develops, hypotension may develop, followed by shock.
B. Laboratory Findings
Leukocytosis or neutrophilia may be present early in the
course. Blood cultures are variably positive. If a central
ulceration, pustule, or abscess is present, culture may be of
value. In immunosuppressed patients, or if an unusual
organism is suspected and there is no loculated site to culture, a full-thickness skin biopsy should be sent for histologic evaluation and culture (bacterial, fungal, and
mycobacterial). If a primary source for the infection is
identified (wound, leg ulcer, toe web intertrigo), cultures
from these sites isolate the causative pathogen in half of
cases and can be used to guide antibiotic therapy.
» Differential Diagnosis
DVT and necrotizing fasciitis are two potentially lifethreatening entities that can mimic cellulitis (ie, present
with a painful, red, swollen lower extremity). Necrotizing
fasciitis should be suspected in a patient who has a toxic
appearance, bullae, crepitus or anesthesia of the involved
skin, skin necrosis, and laboratory evidence of
rhabdomyolysis (elevated creatine kinase) or disseminated
intravascular coagulation. While these findings may be
present with severe cellulitis and bacteremia, it is essential
to rule out necrotizing fasciitis because rapid surgical
debridement is essential. Other noninfectious skin lesions
that may resemble cellulitis are termed “pseudocellulitis.”
These include sclerosing panniculitis, an acute, exquisitely
tender red plaque on the medial lower legs above the malleolus in patients with venous stasis or varicosities, and
acute severe contact dermatitis on a limb, which produces
erythema, vesiculation, and edema, as seen in cellulitis, but
with itching instead of pain. Bilateral lower leg bacterial
cellulitis is exceedingly rare, and other diagnoses, especially severe stasis dermatitis (see Figure 14–2), should be
considered in this setting. In contrast to cellulitis, severe
lower extremity stasis dermatitis usually develops over
days to weeks (rather than hours) and is not as tender to
palpation. Cryptococcal cellulitis in the organ transplant
recipient is often bilateral. The ALT-70 is a predictive
model to diagnose cellulitis or a cellulitis mimic and to
provide guidance about when a dermatology consultation
is needed.
» Treatment
Intravenous or parenteral antibiotics may be required for
the first 2–5 days, with adequate coverage for Streptococcus
and Staphylococcus. Methicillin-susceptible S aureus
(MSSA) can be treated with nafcillin, cefazolin, clindamycin, dicloxacillin, cephalexin, doxycycline, or TMP-SMZ. If
MRSA is suspected or proven, treatment options include
vancomycin, linezolid, clindamycin, daptomycin, doxycycline, or TMP-SMZ. In mild cases or following the initial
parenteral therapy, oral dicloxacillin or cephalexin, 250–
500 mg four times daily for 5–10 days, is usually adequate.
In patients in whom intravenous treatment is not instituted, the first dose of oral antibiotic can be doubled to
achieve high blood levels rapidly. Prior episodes of cellulitis, lymphedema, chronic venous insufficiency, peripheral
vascular disease, and DVT are associated with an increased
risk of recurrent cellulitis. In patients with recurrent lower
leg cellulitis (three to four episodes per year), oral penicillin 250 mg twice daily or oral erythromycin 250–500 mg
twice daily can decrease the risk of recurrence. Additional
measures to prevent recurrences include compression,
treating toe web intertrigo and tinea pedis, and controlling
venous insufficiency.
» When to Admit
• Severe local symptoms and signs.
• Signs of sepsis.
• Elevated WBC count of 10,000/mcL (10 × 109/L) or
more with marked left shift. Failure to respond to oral
antibiotics.
Boettler MA et al. Cellulitis: a review of current practice
guidelines and differentiation from pseudocellulitis. Am J
Clin Dermatol. 2022;23:153. [PMID: 34902109]
Peghin M et al. Prevention and treatment of recurrent cellulitis.
Curr Opin Infect Dis. 2023;36:95. [PMID: 36853755]
DERMATOLOGIC DISORDERS
ERYSIPELAS
ESSENTIALS OF DIAGNOSIS
»
Edematous, circumscribed, hot, erythematous
area, with raised advancing border.
»
Central face or lower extremity frequently
involved.
»
Pain and systemic toxicity may be striking.
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127
» General Considerations
Erysipelas is a superficial form of cellulitis that is usually
caused by beta-hemolytic streptococci.
» Clinical Findings
A. Symptoms and Signs
The symptoms are pain, malaise, chills, and moderate
fever. A bright red patch appears and then spreads to form
a tense, sharply demarcated, glistening, smooth, hot
plaque. The sharp margin characteristically advances
noticeably in days or even hours. The lesion has a raised
edge and may pit slightly with finger pressure. Vesicles or
bullae occasionally develop on the surface. The lesion does
not usually become pustular or gangrenous and heals
without scar formation. Breaks in the skin often provide a
portal of entry for the organism. On the face, erysipelas
begins near a fissure at the angle of the nose. On the lower
extremity, tinea pedis with interdigital fissuring is a common portal of entry.
B. Laboratory Findings
Leukocytosis is almost invariably present; blood cultures
may be positive.
» Differential Diagnosis
Erysipeloid is a benign bacillary infection by Erysipelothrix
rhusiopathiae that produces cellulitis of the skin of the fin-
gers or the backs of the hands in fishermen and meat
handlers.
» Complications
Unless erysipelas is promptly treated, death may result
from bacterial dissemination, particularly in older adults.
» Treatment
Intravenous antibiotics effective against group A betahemolytic streptococci and staphylococci should be considered, but outpatient treatment with oral antibiotics has
demonstrated equal efficacy. Oral regimens include a 7-day
course with penicillin VK (250 mg), dicloxacillin (250 mg),
or a first-generation cephalosporin (250 mg) four times a
day. Clindamycin (250 mg twice daily orally for 7–14 days)
is an option for penicillin-allergic patients.
▲
Figure 6–18. Erythema migrans on trunk. Annular
plaque with central clearing and central puncta from
the bite. (Reproduced, with permission, from Soutor C,
Hordinsky MK. Clinical Dermatology. The McGraw-Hill
Companies; 2013.)
» Prognosis
With appropriate treatment, rapid improvement is
expected. The presence of lymphedema carries the greatest
risk of recurrence.
Oganesyan A et al. From the Cochrane Library: interventions for
cellulitis and erysipelas. JMIR Dermatol. 2022;5:e37888.
[PMID: 37632897]
ERYTHEMA MIGRANS
Erythema migrans is a unique cutaneous eruption that
characterizes the localized or generalized early stage of
Lyme disease (caused by Borrelia burgdorferi) (Figure 6–18)
(see also Chapter 36).
PARASITIC INFESTATIONS
SCABIES
ESSENTIALS OF DIAGNOSIS
»
Generalized very severe itching; infestation usually spares the head and neck.
»
Burrows, vesicles, and pustules, especially on finger webs and in wrist creases.
»
Mites, ova, and brown dots of feces (scybala) visible microscopically.
»
Red papules or nodules on the scrotum and on
the penile glans and shaft are pathognomonic.
» General Considerations
Scabies is caused by infestation with Sarcoptes scabiei,
affecting over 200 million persons worldwide. Close physical contact for 15–20 minutes with an infected person is
128
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the typical mode of transmission. However, scabies may be
acquired by contact with the bedding of an infested individual. Facility-associated scabies is common, primarily in
long-term care facilities, and misdiagnosis is common.
Index patients are usually older adults and immunosuppressed. When these patients are hospitalized, hospitalbased epidemics can occur and are difficult to eradicate
when health care workers become infected and spread the
infestation to other patients.
» Clinical Findings
A. Symptoms and Signs
Itching is almost always present and can be severe. The
lesions consist of generalized excoriations with small pruritic vesicles, pustules, and “burrows” in the interdigital
spaces of the hands and feet, on the heels of the palms,
wrists, elbows, umbilicus, around the axillae, on or around
the areolae (Figure 6–19), or on the penile shaft and scrotum in men. The burrow appears as a short irregular mark,
2–3 mm long and the width of a hair. Characteristic nodular lesions may occur on the scrotum or penis and along
the posterior axillary line. The infestation usually spares
the head and neck (though these areas may be involved in
infants, older adults, and patients with AIDS).
Hyperkeratotic or crusted scabies presents as thick flaking scale. These areas contain millions of mites, and these
patients are highly infectious. Pruritus is often absent.
Patients with widespread hyperkeratotic scabies are at risk
for superinfection with S aureus, which in some cases pro-
gresses to sepsis if left untreated. Crusted scabies is the
cause of 83% of scabies outbreaks in institutions.
B. Laboratory Findings
The diagnosis should be confirmed by microscopic demonstration of the organism, ova, or feces in a mounted
specimen, examined with tap water, mineral oil, or KOH.
Best results are obtained when multiple lesions are scraped,
choosing the best unexcoriated lesions from interdigital
webs, wrists, elbows, or feet. A No. 15 blade is used to
▲
Figure 6–19. Scabies. A polymorphic eruption of
papulovesicles and excoriated papules scattered on the
chest. (Used, with permission, from Kanade Shinkai, MD.)
scrape each lesion until it is flat. Patients with crusted/
hyperkeratotic scabies must be evaluated for immunosuppression (especially HIV and HTLV-1 infections) if no
iatrogenic cause of immunosuppression is present.
» Differential Diagnosis
Scabies must be distinguished from the various forms of
pediculosis, from bedbug and flea bites, and from other
causes of pruritus.
» Treatment & Prognosis
Treatment is aimed at killing scabies mites and controlling
the dermatitis, which can persist for months after effective
eradication of the mites. Bedding and clothing should be
laundered or set aside for 14 days in plastic bags. High heat
(60°C) is required to kill the mites and ova. Treatment is
aimed at all infected persons in a family or institutionalized
group. Otherwise, reinfestations will likely occur, which is
why scabies in nursing home patients, institutionalized or
patients with a mental illness, and patients with AIDs may
be much more difficult to treat.
1. Permethrin 5% cream—Treatment with permethrin, a
highly effective and safe agent, consists of a single application from the neck down for 8–12 hours then washed off,
repeated in 1 week. Patients often continue to itch for several weeks after treatment. Use of triamcinolone 0.1%
cream helps resolve the dermatitis.
Pregnant patients should be treated only if they have
documented scabies. Permethrin 5% cream once for
12 hours or 5% or 6% sulfur in petrolatum applied nightly
for 3 nights from the neck down may be used.
Most failures in normal persons are related to incorrect
use or incomplete treatment of the housing unit. In these
cases, repeat treatment with permethrin once weekly for
2 weeks, with re-education regarding the method and
extent of application, is suggested.
2. Ivermectin—In immunocompetent individuals, 200 mcg/kg
orally is effective in about 75% of cases with a single dose
and in 95% of cases with two doses 2 weeks apart. Since the
drug is not ovicidal, the second dose theoretically kills eggs
that might have hatched after the first dose was given.
Ivermectin is often used in combination with permethrin. In immunosuppressed persons and those with
crusted (hyperkeratotic) scabies, multiple doses of ivermectin (every 2 weeks for 2 or 3 doses) plus topical therapy
with permethrin every 3 days to once weekly, depending
on degree of involvement, may be effective when topical
treatment and oral therapy alone fail. A topical keratolytic
(urea) should be used to help remove the scale of hyperkeratotic scabies, thereby decreasing the mite load.
Ivermectin can be beneficial in mass treatment to eradicate widespread infection. In endemic areas, mass intervention with ivermectin is effective in controlling both
scabies and associated bacterial infections.
3. Spinosad—For treatment-resistant patients, 0.9% spinosad suspension, applied once over a time period longer
than 6 hours, can be considered, though efficacy is lower
than that for ivermectin or permethrin.
DERMATOLOGIC DISORDERS
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129
Richards RN. Scabies: diagnostic and therapeutic update. J Cutan
Med Surg. 2021;25:95. [PMID: 32998532]
Widaty S et al. Scabies: update on treatment and efforts for
prevention and control in highly endemic settings. J Infect
Dev Ctries. 2022;16:244. [PMID: 35298417]
PEDICULOSIS
ESSENTIALS OF DIAGNOSIS
»
Pruritus with excoriation.
»
Nits on hair shafts; lice on skin or clothes.
»
Occasionally, sky-blue macules (maculae ceruleae)
on the inner thighs or lower abdomen in pubic
lice infestation.
» General Considerations
Pediculosis is a parasitic infestation of the skin of the scalp,
trunk, or pubic areas. Body lice usually occur among persons who live in overcrowded dwellings with inadequate
hygiene facilities. Pubic lice may be sexually transmitted.
Head lice may be transmitted by shared use of hats or
combs. Adults in contact with children with head lice frequently acquire the infestation.
There are three different varieties: (1) pediculosis capi-
tis, caused by Pediculus humanus var capitis (head louse);
(2) pediculosis corporis, caused by Pediculus humanus var
corporis (body louse); and (3) pediculosis pubis, caused by
Phthirus pubis (pubic louse, “crabs”).
Head and body lice are 3–4 mm long and similar in
appearance. The “body louse” can seldom be found on the
body because it comes onto the skin only to feed; it must be
looked for in the seams of the clothing. Trench fever,
relapsing fever, and typhus are transmitted by the body
louse in countries where those diseases are endemic. In the
United States, Bartonella quintana, the organism that
causes trench fever, has been found in lice infesting persons
with housing instability.
» Clinical Findings
In body lice infestations, itching may be very intense, and
scratching may result in deep excoriations, especially over
the upper shoulders, axillae, posterior flanks, and neck. In
some cases, only itching is present, with few excoriations
seen. Pyoderma (bacterial infection of the skin) may be the
presenting sign. Diagnosis is made by examining the seams
of clothing for nits and lice. Head lice presents as scalp
pruritus often accompanied by erosions on the occipital
scalp, posterior neck, and upper back. Diagnosis is made by
finding lice on the scalp or small nits resembling pussy willow buds on the scalp hairs close to the skin. Nits are easiest
to see above the ears and at the nape of the neck. Pubic lice
infestations are occasionally generalized, particularly in
hairy individuals; the lice may even be found on the eyelashes and in the scalp. Diagnosis is made by finding lice or
nits on pubic hair, body hair, or eyelashes.
» Differential Diagnosis
Head lice infestation must be distinguished from seborrheic dermatitis, body lice infestation from scabies and
bedbug bites, and pubic lice infestation from anogenital
pruritus and eczema.
» Treatment
1. Pediculosis capitis—Permethrin 1% cream rinse (Nix)
is a topical over-the-counter pediculicide and ovicide. It is
applied to the scalp and hair and left on for 8 hours before
being rinsed off. Although it is the treatment of choice for
head lice, permethrin resistance is common. Malathion
lotion 1% (Ovide) is very effective but highly volatile and
flammable, so application must be done in a well-ventilated
room or out of doors. Topical ivermectin 0.5% lotion, benzyl alcohol 5%, Oxyphthirine® lotion, spinosad 0.9% suspension, dimethicone, and abametapir 0.74% lotion are
additional agents that have efficacy against pediculosis
capitis; of these, topical ivermectin is the most effective. All
infested persons in a household, school, or other facility
should ideally be treated at the same time. Other than topical ivermectin, topical therapies should be repeated
7–9 days after the initial treatment. For involvement of
eyelashes, petrolatum is applied thickly twice daily for
8 days and the remaining nits plucked off. Systemic treatment options, often used in combination with topical
agents, are oral ivermectin (200 mcg/kg orally, repeated in
7 days) (for children older than 5 years and more than 15 kg)
and oral TMP-SMZ (10 mg TMP/kg/day and 50 mg SMZ/
kg/day divided twice daily for 10 days).
2. Pediculosis corporis—Body lice are treated by disposing
of the infested clothing and addressing the patient’s social
situation.
3. Pediculosis pubis—Application of permethrin rinse 1%
for 10 minutes or permethrin cream 5% for 8 hours to the
pubis is effective. Sexual contacts should be treated. Clothes
and bedclothes should be washed and dried at high
temperature.
Fu YT et al. Human pediculosis, a global public health problem.
Infect Dis Poverty. 2022;11:58. [PMID: 35619191]
Patel PU et al. A clinical review and history of pubic lice.
Clin Exp Dermatol. 2021;46:1181. [PMID: 33811771]
SKIN LESIONS DUE TO OTHER ARTHROPODS
ESSENTIALS OF DIAGNOSIS
»
Localized urticarial papules with pruritus.
»
Lesions in linear groups of three (“breakfast, lunch,
and dinner”) are characteristic of bedbugs.
»
Furuncle-like lesions containing live arthropods.
»
Tender erythematous patches that migrate (“larva
migrans”).
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» General Considerations
Some arthropods (eg, mosquitoes and biting flies) are
readily detected as they bite. Many others are not because
they are too small, because there is no immediate reaction,
or because they bite during sleep. Reactions are allergic and
may be delayed for hours to days. Patients are most apt to
consult a clinician when the lesions are multiple and pruritus is intense.
Many persons react most severely to their earliest contacts with an arthropod, thus presenting with pruritic lesions
when traveling, moving into new quarters, etc. Body lice,
fleas, bedbugs, and mosquitoes should be considered. Bedbug exposure typically occurs in hotels and in housing with
inadequate hygiene but also occurs in stable domiciles. Spiders are often incorrectly believed to be the source of bites,
but they rarely attack humans. However, the brown recluse
spider (Loxosceles laeta, L reclusa) may cause severe necrotic
reactions and death due to intravascular hemolysis, and the
black widow spider (Latrodectus mactans) may cause severe
systemic symptoms and death. (See also Chapter 40.)
In addition to arthropod bites, the most common
lesions are venomous stings (wasps, hornets, bees, ants,
scorpions) or bites (centipedes), furuncle-like lesions due
to fly maggots or sand fleas in the skin, and a linear creeping eruption due to a migrating larva.
» Clinical Findings
The diagnosis may be difficult when the patient has not
noticed the initial attack but suffers a delayed reaction.
Individual bites are often in clusters and tend to occur
either on exposed parts (eg, midges and gnats) or under
clothing, especially around the waist or at flexures (eg,
small mites or insects in bedding or clothing). The reaction
is often delayed for 1–24 hours or more. Pruritus is almost
always present and may be all but intolerable once the
patient starts to scratch. Secondary infection may follow
scratching. Urticarial wheals are common. Papules may
become vesicular. The diagnosis is aided by searching for
exposure to arthropods and by considering the patient’s
occupation and recent activities.
The principal arthropods are as follows:
1. Fleas: Fleas are bloodsucking ectoparasites that feed on
dogs, cats, humans, and other species. Flea saliva pro-
duces papular urticaria in sensitized individuals. To
break the life cycle of the flea, one must treat the home
and pets, using quick-kill insecticides, residual insecti-
cides, and a growth regulator.
2. Bedbugs: In crevices of beds or furniture; bites tend to
occur in lines or clusters. Papular urticaria is a character-
istic lesion of bedbug (Cimex lectularius) bites. Bedbugs
are not restricted to any socioeconomic group and are a
major health problem in some major metropolitan areas,
especially in commercial and residential hotels.
3. Ticks: Usually picked up by brushing against low vege-
tation.
4. Chiggers or red bugs: These are larvae of trombiculid
mites. A few species confined to particular regions and
locally recognized habitats (eg, berry patches, woodland
edges, lawns, brush turkey mounds in Australia, poultry farms) attack humans, often around the waist, on
the ankles, or in flexures, raising intensely itching erythematous papules after a delay of many hours. The red
chiggers may sometimes be seen in the center of papules that have not yet been scratched.
5. Bird and rodent mites: Larger than chiggers, bird mites
infest birds and their nests. Bites are multiple anywhere
on the body. Room air conditioning units may transmit
outdoor bird mites to inhabitants of the room. Rodent
mites from mice or rats may cause similar effects. If the
domicile has evidence of rodent activity, then rodent
mite dermatitis should be suspected, as the mites are
rarely found. Pet rodents or birds may be infested with
mites, maintaining the infestation.
6. Mites in stored products: These are white and almost
invisible and infest products, such as copra, vanilla
pods, sugar, straw, cottonseeds, and cereals. Persons
who handle these products may be attacked, especially
on the hands and forearms and sometimes on the feet.
7. Caterpillars of moths with urticating hairs: The hairs
are blown from cocoons or carried by emergent moths,
causing severe and often seasonally recurrent outbreaks
after mass emergence. The gypsy moth is a cause in the
eastern United States.
8. Tungiasis: Tungiasis is due to the burrowing flea
known as Tunga penetrans and is found in Africa, the
West Indies, and South and Central America. The
female burrows under the skin, sucks blood, swells to
0.5 cm, and then ejects her eggs onto the ground.
Ulceration, lymphangitis, gangrene, and septicemia
may result, in some cases with lethal effect. Simple surgical removal is usually performed.
» Prevention
Arthropod infestations are best prevented by avoidance of
contaminated areas, personal cleanliness, and disinfection
of clothing, bedclothes, and furniture as indicated. Chiggers and mites can be repelled by permethrin applied to the
head and clothing. (It is not necessary to remove clothing.)
Bedbugs are no longer repelled by permethrin and can
survive for up to 1 year without feeding. Aggressive cleaning, usually requiring removal of the affected occupant
from the domicile, may be necessary to eradicate bedbug
infestation in a residence.
» Treatment
Living arthropods should be removed carefully with tweezers after application of alcohol and preserved in alcohol
for identification. In endemic Rocky Mountain spotted
fever areas, ticks should not be removed with the bare
fingers.
Corticosteroid lotions or creams are helpful for the
associated pruritus. Topical antibiotics may be applied if
secondary infection is suspected. Localized persistent
lesions may be treated with intralesional corticosteroids.
Stings produced by many arthropods may be alleviated
by applying papain powder (Adolph’s Meat Tenderizer)
DERMATOLOGIC DISORDERS
mixed with water, or aluminum chloride hexahydrate
(Xerac AC).
Extracts from venom sacs of bees, wasps, yellow jackets,
and hornets are available for immunotherapy of patients at
risk for anaphylaxis.
Parola P et al. Bedbugs. N Engl J Med. 2020;382:2230. [PMID:
32492304]
º
INFLAMMATORY NODULES
ERYTHEMA NODOSUM
ESSENTIALS OF DIAGNOSIS
»
Painful nodules without ulceration on anterior
aspects of legs.
»
Slow regression over several weeks to resemble
contusions.
»
Women are predominantly affected by a ratio of
10:1 compared to men.
»
Some cases associated with infection, IBD, or
medication exposure.
»
Evaluation for underlying cause is essential.
CMDT 2025
131
» General Considerations
Erythema nodosum is a symptom complex of panniculitis
characterized by tender, erythematous nodules that appear
most commonly on the extensor surfaces of the lower legs.
It usually lasts about 6 weeks and may recur. Most cases are
idiopathic in nature. However, erythema nodosum can be
a skin sign of systemic disease. Evaluation and management include making the diagnosis, treating the symptoms,
and searching for an underlying cause. The disease may be
associated with various infections—streptococcosis, primary coccidioidomycosis, other deep fungal infections,
tuberculosis, Yersinia pseudotuberculosis and Y enterocolit-
ica infection, Salmonella and other GI pathogens, diverticulitis, or syphilis. It may accompany sarcoidosis, Behçet
disease, and IBD. Erythema nodosum may be associated
with pregnancy or with use of oral contraceptives. It may
occur secondary to medications or, more rarely, an underlying malignancy.
» Clinical Findings
A. Symptoms and Signs
The subcutaneous swellings are exquisitely tender and may
be preceded by fever, malaise, and arthralgia. They are
most often located on the anterior surfaces of the legs
below the knees but may occur on the arms, trunk, and
face. The lesions, 1–10 cm in diameter, are at first pink to
red; with regression, all the various hues seen in a contusion can be observed (Figure 6–20) but, as a rule, the
lesions do not ulcerate.
▲
Figure 6–20. Erythema nodosum. (Used, with
permission, from TG Berger, MD, Dept Dermatology, UCSF.)
B. Laboratory Findings
Evaluation of patients presenting with acute erythema
nodosum should include a careful history (including
medication exposures) and physical examination. Significant findings include a history of prior upper respiratory
infection, diarrheal illness, exposure to tuberculosis, or
symptoms of any deep fungal infection endemic to the
area. In patients lacking an obvious drug or medical
cause, a CXR, a purified protein derivative or blood interferon gamma release assay (such as QuantiFERON) (see
Pulmonary Tuberculosis in Chapter 9), and two consecutive ASO/DNAse B titers at 2- to 4-week intervals should
be obtained. Coccidioidomycosis should be looked for in
patients from endemic areas. If no underlying cause is
found, only a small percentage of patients will go on to
develop a significant underlying illness over the next year.
» Differential Diagnosis
Unlike other forms of panniculitis, a defining feature of
erythema nodosum is that it does not ulcerate.
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Erythema induratum from tuberculosis is seen on the posterior surfaces of the legs and may ulcerate. Lupus panniculitis presents as tender nodules in fatty areas of the
buttocks and posterior arms and heals with depressed
scars. In polyarteritis nodosa, the subcutaneous nodules
are often associated with fixed livedo reticularis. In its late
stages, erythema nodosum must be distinguished from
simple bruises and contusions.
» Treatment
The underlying cause should be identified and treated.
Primary therapy is with NSAIDs in usual doses. Saturated
solution of potassium iodide, 5–15 drops by mouth three
times daily, results in prompt involution in many cases.
Complete bed rest may be advisable if the lesions are painful. Systemic therapy directed against the lesions themselves may include corticosteroid therapy (see Chapter 28)
(unless contraindicated by associated infection), dapsone,
colchicine, or hydroxychloroquine.
» Prognosis
The lesions usually disappear after about 6 weeks but may
recur.
Pérez-Garza DM et al. Erythema nodosum: a practical approach
and diagnostic algorithm. Am J Clin Dermatol. 2021;22:367.
[PMID: 33683567]
º
SCALING DISORDERS
ATOPIC DERMATITIS
ESSENTIALS OF DIAGNOSIS
»
Pruritic, xerotic, exudative, or lichenified eruption
on face, neck, upper trunk, wrists, and hands and
in the antecubital and popliteal folds.
»
Personal or family history of atopy (eg, asthma,
allergic rhinitis, atopic dermatitis).
»
Tendency to recur.
»
Onset in childhood most common; onset after age
30 is uncommon.
» General Considerations
Atopic dermatitis (also known as eczema) has distinct presentations in persons of different ages and races. Diagnostic criteria for atopic dermatitis must include pruritus,
typical morphology and distribution (flexural lichenification, hand eczema, nipple eczema, and eyelid eczema in
adults), onset in childhood, and chronicity. Also helpful are
(1) a personal or family history of atopy (asthma, allergic
rhinitis, atopic dermatitis), (2) xerosis-ichthyosis, (3) facial
pallor with infraorbital darkening, (4) elevated serum IgE,
and (5) repeated skin infections.
» Clinical Findings
A. Symptoms and Signs
Itching is a key clinical feature and may be severe and prolonged. Ill-defined, scaly, red plaques affect the face, neck,
and upper trunk. The flexural surfaces of elbows and knees
are often involved. In chronic cases, the skin is dry and
lichenified. In patients with darker skin with severe disease, pigmentation may be lost in lichenified areas. During
acute flares, widespread redness with weeping, either diffusely or in discrete plaques, is common. Virtually all
patients with atopic dermatitis have skin disease before age
5; therefore, a new diagnosis of atopic dermatitis in an
adult over age 30 should be made only after consultation
with a dermatologist.
B. Laboratory Findings
Food allergy is an uncommon cause of flares of atopic dermatitis in adults. Eosinophilia and increased serum IgE
levels may be present.
» Differential Diagnosis
Atopic dermatitis must be distinguished from irritant or
allergic contact dermatitis. Seborrheic dermatitis is less
pruritic, with frequent scalp and central face involvement,
greasy and scaly lesions, and responds quickly to therapy.
Psoriasis is marked by sharply demarcated thickly scaled
plaques on elbows, knees, scalp, and intergluteal cleft. Secondary staphylococcal or herpetic infections may exacerbate atopic dermatitis and should be considered during
hyperacute, weeping flares. An infra-auricular fissure is a
cardinal sign of secondary staphylococcal infection.
» Treatment
Patient education regarding gentle skin care and proper use
of medications is critical to successful management of
atopic dermatitis.
A. General Measures
Atopic patients have hyperirritable skin. Anything that dries
or irritates the skin may trigger dermatitis. Atopic individuals are sensitive to low humidity and often flare in the winter.
Adults with atopic disorders should not bathe more than
once daily. Soap should be confined to the armpits, groin,
scalp, and feet. Washcloths and brushes should not be used.
After rinsing, the skin should be patted dry (not rubbed)
and then immediately—within minutes—covered with a
thin film of an emollient or a corticosteroid as needed. Plain
petrolatum can be used if contact dermatitis resulting from
additives in medication is suspected. Skin may be irritated
by rough fabrics, including wools and acrylics. Cottons are
preferable, but synthetic blends also are tolerated. Other
triggers may include sweating, ointments, and heat.
B. Local Treatment
Corticosteroids should be applied sparingly to the dermatitis once or twice daily. Their potency should be appropriate to the severity of the dermatitis. In general, for
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133
treatment of lesions on the body (excluding genitalia, axillary or crural folds), one should begin with triamcinolone
0.1% or a stronger corticosteroid, then taper to hydrocortisone or another slightly stronger mild corticosteroid (alclometasone, desonide). It is vital that patients taper off
corticosteroids and substitute emollients as the dermatitis clears to avoid side effects of corticosteroids. Tapering
is also important to avoid dermatitis flares that may follow
abrupt cessation. Tacrolimus ointment (Protopic 0.03% or
0.1%), pimecrolimus cream (Elidel 1%), crisaborole
(Eucrisa 2%), and ruxolitinib (Opzelura 1.5%) are nonsteroidal topical medications that may be effective in managing atopic dermatitis when applied twice daily (see
Table 6–2). These noncorticosteroid medications prevent
complications of long-term corticosteroid use, including
atrophy or striae. They are safe for application on the face
and eyelids but are more expensive than generic topical
corticosteroids.
There is a US FDA black box warning for both topical
tacrolimus and pimecrolimus due to concerns about the
development of T-cell lymphoma. A systematic review and
meta-analysis found a weak association between topical
calcineurin inhibitor use and lymphoma; however, the absolute risk is very low. The number needed to harm is estimated
at 30,000 adults and 200,000 children.
The treatment of atopic dermatitis is dictated by the
pattern of the dermatitis—acute/weepy, subacute/scaly, or
chronic/lichenified.
detergens 10% in Aquaphor or 2% crude coal tar may be
beneficial.
4. Maintenance treatment—Once symptoms have
improved, constant application of effective moisturizers is
recommended to prevent flares. In patients with moderate
disease, use of topical anti-inflammatories only on weekends or three times weekly can prevent flares.
C. Systemic and Adjuvant Therapy
Increasingly, providers try to avoid the use of systemic
steroids in the treatment of atopic dermatitis. Systemic
corticosteroids are indicated only for severe acute exacerbations. Oral prednisone dosages should be high enough to
suppress the dermatitis quickly, usually starting with 1 mg/
kg daily and tapering off over a period of 2–4 weeks.
Owing to the chronic nature of atopic dermatitis and the
side effects of long-term systemic corticosteroids, ongoing
use of these agents is not recommended for maintenance
therapy. Bedtime doses of hydroxyzine, diphenhydramine,
or doxepin may be helpful via their sedative properties to
mitigate perceived pruritus. Dupilumab and the newer
IL-13 inhibitor tralokinumab are targeted immunomodulators with minimal systemic adverse effects (hypersensitivity). Janus kinase (JAK) inhibitors (upadacitinib,
abrocitinib), cyclosporine, mycophenolate mofetil, methotrexate, or azathioprine may also be used for the most
severe and recalcitrant cases.
1. Acute weeping lesions—Staphylococcal or herpetic
superinfection should be excluded by bacterial or viral
culture, or both. Use water or aluminum subacetate solution (Domeboro or burow solution), or colloidal oatmeal
as a bath or as wet dressings for 10–30 minutes two to four
times daily. Lesions on extremities may be bandaged for
protection at night. Use high-potency corticosteroids after
soaking but spare the face and body folds. Tacrolimus is
usually not tolerated at this stage. Systemic corticosteroids
may be required. An allergic or irritating contactant should
also be considered when acute weeping lesions are present
since contact dermatitis is more likely to develop in atopic
patients.
2. Subacute or scaly lesions—The lesions are dry but still
red and pruritic. Mid- to high-potency corticosteroids in
ointment form should be continued until skin lesions are
cleared and itching is decreased substantially. At that point,
patients should begin a 2- to 4-week taper from twice-daily
to daily dosing with topical corticosteroids to reliance on
emollients, with occasional use of corticosteroids only to
inflamed areas. It is preferable to switch to daily use of a
low-potency corticosteroid instead of further tapering the
frequency of usage of a more potent corticosteroid. Tacrolimus and pimecrolimus may be substituted if corticosteroids cannot be stopped completely.
3. Chronic, dry, lichenified lesions—Thickened and usually well demarcated, they are best treated with highpotency to ultra–high-potency corticosteroid ointments.
Nightly occlusion for 2–6 weeks may enhance the initial
response. Adding tar preparations, such as liquor carbonis
» Complications of Treatment
The clinician should monitor for skin atrophy. Fissures,
crusts, erosions, or pustules may indicate staphylococcal or
herpetic infection clinically. Eczema herpeticum (herpes
simplex superinfection) is manifested by monomorphic
vesicles, crusts, or scalloped erosions superimposed on
atopic dermatitis or other extensive eczematous processes
and is treated with oral or intravenous acyclovir. Systemic
antistaphylococcal antibiotics should be given only if indicated and guided by bacterial culture. Cultures to exclude
methicillin-resistant S aureus are recommended. In this
setting, continuing and augmenting the topical antiinflammatory treatment often improves the dermatitis
despite the presence of infection.
» Prognosis
Atopic dermatitis runs a chronic or intermittent course.
Affected adults may have only hand dermatitis. Prognostic
factors for persistence into adulthood include generalized
disease or onset early in childhood and asthma. Only
40–60% of these patients have lasting remissions.
Clebak KT et al. Atopic dermatitis. Prim Care. 2023;50:191.
[PMID: 37105601]
Drucker AM et al. Systemic immunomodulatory treatments for
atopic dermatitis: update of a living systematic review and
network meta-analysis. JAMA Dermatol. 2022;158:523.
[PMID: 35293977]
Schuler CF 4th et al. Novel insights into atopic dermatitis.
J Allergy Clin Immunol. 2023;151:1145. [PMID: 36428114]
134
CMDT 2025
CHAPTER 6
LICHEN SIMPLEX CHRONICUS
Circumscribed Neurodermatitis
ESSENTIALS OF DIAGNOSIS
»
Chronic itching and scratching.
»
Lichenified lesions with exaggerated skin lines
overlying a thickened, well-circumscribed, scaly
plaque.
»
Predilection for nape of neck, wrists, external surfaces of forearms, lower legs, and genitals.
» General Considerations
Lichen simplex chronicus represents a self-perpetuating
scratch-itch cycle that is hard to disrupt.
» Clinical Findings
Intermittent itching incites the patient to scratch the
lesions and may interfere with sleep. Dry, hypertrophic,
lichenified plaques appear on the neck, wrists, ankles, or
perineum (Figure 6–21). The patches are rectangular,
thickened, and hyperpigmented. The skin lines are
exaggerated.
» Differential Diagnosis
This disorder can be differentiated from plaque-like lesions
such as psoriasis (redder lesions having whiter scales on
the elbows, knees, and scalp and nail findings) (Figure 6–22),
lichen planus (violaceous, usually smaller polygonal papules), and nummular (coin-shaped) dermatitis. Lichen
simplex chronicus may complicate chronic atopic dermatitis or scabetic infestation.
» Treatment
For lesions in extragenital regions, ultra-high potency
topical corticosteroids are effective, with or without
▲
Figure 6–22. Extensive plaque psoriasis involving
trunk of person with dark skin type. (Used, with permission, from Kanade Shinkai, MD.)
occlusion, when used twice daily for several weeks
(Table 6–2). In some patients, flurandrenolide (Cordran)
tape may be effective since it prevents scratching and rubbing of the lesion. The injection of triamcinolone acetonide suspension (5–10 mg/mL) into the lesions may
occasionally be curative. Continuous occlusion with a
flexible hydrocolloid dressing for 7 days at a time for
1–2 months may also be helpful. For genital lesions, see
the section Pruritus Ani.
» Prognosis
The disease tends to remit during treatment but may recur
or develop at another site.
Juarez MC et al. A systematic review of evidence based treat-
ments for lichen simplex chronicus. J Dermatolog Treat.
2021;32:684. [PMID: 31884840]
Starace M et al. Scalp dysaesthesia and lichen simplex chronicus:
diagnostic and therapeutic update with literature review. Clin
Exp Dermatol. 2022;47:3. [PMID: 34137059]
PSORIASIS
▲
Figure 6–21. Lichen simplex chronicus on the hand.
(Used, with permission, from Lindy Fox, MD.)
ESSENTIALS OF DIAGNOSIS
»
Silvery scales on bright red, well-demarcated
plaques, usually on the knees, elbows, and scalp.
»
Nails: pitting and onycholysis (separation of the
nail plate from the bed).
»
Mild itching is common.
»
May be associated with psoriatic arthritis.
»
Histopathology is helpful.
» General Considerations
Psoriasis is a common benign, chronic inflammatory
skin disease with both a genetic basis and known
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135
environmental triggers. Injury or irritation of normal skin
tends to induce lesions of psoriasis at the site (Koebner
phenomenon). Obesity worsens psoriasis, and significant
weight loss may lead to substantial improvement. Psoriasis
has several variants—the most common is the plaque type,
and hand involvement is also common. Eruptive (guttate)
psoriasis consisting of numerous, smaller lesions 3–10 mm
in diameter occurs occasionally after streptococcal
pharyngitis. Rarely, life-threatening forms (generalized
pustular psoriasis and erythrodermic psoriasis) may
occur.
» Clinical Findings
There are often no symptoms, but itching may occur and
be severe. Favored sites include the scalp, elbows, knees,
palms and soles, and nails. The lesions are red, sharply
defined plaques covered with silvery scale (Figure 6–22).
The glans penis and vulva may be affected. Occasionally,
only the flexures (axillae, inguinal areas) are involved
(termed inverse psoriasis). Fine stippling (“pitting”) in the
nails is highly suggestive of psoriasis (Figure 6–23) as is
onycholysis. The combination of red plaques with silvery
scales on elbows and knees, with scaliness in the scalp or
nail findings, is diagnostic. Patients with psoriasis often
have a pink or red intergluteal fold. Not all patients have
findings in all locations. Some patients have mainly hand
or foot psoriasis with minimal findings elsewhere. There
may be associated arthritis that is most commonly distal
and oligoarticular, although polyarticular, axial, and arthritis mutilans involvement may occur. The psychosocial
impact of psoriasis is a major factor in determining the
treatment of the patient.
» Differential Diagnosis
Psoriasis lesions are well demarcated and affect extensor
surfaces—in contrast to atopic dermatitis, with poorly
demarcated plaques in flexural distribution. In body
▲
Figure 6–23. Nail pitting due to psoriasis in a
patient with dark skin. (Reproduced with permission
from Richard P. Usatine, MD, in Usatine RP, Smith MA,
Mayeaux EJ Jr, Chumley H. The Color Atlas of Family
Medicine, 2nd ed. McGraw-Hill, 2013.)
folds, scraping and culture for Candida and examination
of scalp and nails will distinguish inverse psoriasis from
intertrigo and candidiasis. Dystrophic changes in nails
may mimic onychomycosis, and a KOH preparation or
fungal culture is valuable in diagnosis. The cutaneous
features of reactive arthritis, pityriasis rosea, SLE, and
syphilis mimic psoriasis.
» Treatment
There are many therapeutic options in psoriasis to be chosen according to the extent (body surface area [BSA]
affected) and the presence of other findings (for example,
arthritis). Certain medications, such as beta-blockers, antimalarials, statins, lithium, and prednisone tapering, may
flare or worsen psoriasis. Patients with moderate to severe
psoriasis should be managed by or in conjunction with a
dermatologist.
A. Limited Disease
For patients with large plaques and less than 10% of the
BSA involved, the easiest regimen is to use a high-potency
to ultra–high-potency topical corticosteroid cream or
ointment. It is best to restrict the ultra–high-potency corticosteroids to 2–3 weeks of twice-daily use and then use
them in a pulse fashion three or four times on weekends
or switch to a mid-potency corticosteroid. Topical corticosteroids rarely induce a lasting remission. Initially, patients
may be treated with twice-daily topical corticosteroids
plus a vitamin D analog (calcipotriene ointment 0.005% or
calcitriol ointment 0.003%) twice daily. This rapidly clears
the lesions; eventually, the topical corticosteroids are
stopped, and once- or twice-daily application of the
vitamin D analog is continued long-term. Calcipotriene
usually cannot be applied to the groin or face because of
irritation. Treatment of extensive psoriasis with vitamin D
analogs may result in hypercalcemia so that the maximum
dose for calcipotriene is 100 g/week and for calcitriol it is
200 g/week. Calcipotriene is incompatible with many topical corticosteroids (but not halobetasol), so if used concurrently, it must be applied at a different time. For
patients with numerous small papules and plaques, such as
guttate psoriasis, narrowband UVB phototherapy is the
best therapy.
For thick plaques on the scalp, start with a daily tar
shampoo. Additional treatments include 6% salicylic acid
gel (eg, Keralyt), P & S solution (phenol, mineral oil, and
glycerin), or fluocinolone acetonide 0.01% in oil (DermaSmoothe/FS) under a shower cap at night, and shampoo in
the morning. In order of increasing potency, triamcinolone
0.1%, fluocinolone, betamethasone dipropionate, amcinonide, and clobetasol are available in solution form for
use on the scalp twice daily. Tacrolimus ointment 0.1% or
0.03% or pimecrolimus cream 1% may be effective in intertriginous, genital, and facial psoriasis, where potent corticosteroids are not recommended due to skin atrophy. Two
additional nonsteroidal topical therapies approved to treat
psoriasis are roflumilast cream 0.3% (phosphodiesterase-4
inhibitor) and tapinarof cream 1% (aryl hydrocarbon
receptor agonist).